CD43, a molecule defective in Wiskott-Aldrich syndrome, binds ICAM-1

@article{Rosenstein1991CD43AM,
  title={CD43, a molecule defective in Wiskott-Aldrich syndrome, binds ICAM-1},
  author={Yvonne Rosenstein and John K. Park and William C. Hahn and Fred S. Rosen and Barbara E. Bierer and Steven J. Burakoff},
  journal={Nature},
  year={1991},
  volume={354},
  pages={233-235}
}
THE protein CD43 (also known as sialophorin, leukosialin, large sialoglycoprotein or gp115) is expressed on the surface of T lymphocytes, monocytes, neutrophils, platelets and some B lymphocytes1–6. Expression of CD43 is deficient and/or defective in the X-chromosome-linked immunodeficiency disorder Wiscott-Aldrich syndrome7, suggesting that CD43 might have a role in T-cell activation. We have shown that expression of human CD43 in an HLA-DR-specific murine T-cell hybridoma enhances the antigen… 
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TLDR
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TLDR
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CD43 Functions as a Ligand for E-Selectin on Activated T Cells1
TLDR
Results suggest that CD43, when modified by a specific set of glycosyltranferases, can function as an E-selectin ligand and therefore potentially mediate activated T cell migration into inflamed sites.
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TLDR
It is observed that CD43 enhances the antigen-specific activation of T cells and that the intracellular domain of CD43, which is hyperphosphorylated during T-cell activation19–21, is required for this function.
Mechanism of mononuclear cell activation by an anti-CD43 (sialophorin) agonistic antibody.
TLDR
It is concluded that CD43 is functionally coupled to the phospholipase C/phosphoinositides signaling pathway in human T cells, and a mutant derived from the leukemic T cell line HPB-ALL that was severely defective in TCR/CD3 surface expression and signaling nevertheless had normal CD43 surface expression compared with the parent cell line.
Sialophorin, a surface sialoglycoprotein defective in the Wiskott- Aldrich syndrome, is involved in human T lymphocyte proliferation
TLDR
Observations suggest that sialophorin functions in T cell activation in patients with the X-linked immunodeficiency Wiskott-Aldrich syndrome.
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TLDR
The ability of purified LFA-3 and anti-CD2 mAb to induce changes in intracellular cAMP content in murine Ag-specific T cell hybridomas that stably express wild-type and mutated human CD2 molecules is studied and suggests that CD2/LFA- 3 interactions may regulate T cell function at least in part through the generation of intrace cellular cAMP.
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TLDR
Evidence for multiple counter-receptors for LFA-1 in the mouse as well as in the human is provided and increased adhesiveness for ICAM-1 stimulated by phorbol esters could be demonstrated for hybrid L FA-1 molecules with human alpha and murine beta subunits.
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TLDR
It is concluded that ICAM-1 is a counter receptor for Mac-1 and that this receptor pair is responsible, in part, for the adhesion between stimulated neutrophils and stimulated endothelial cells.
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TLDR
It is proposed that ICAM-1 may be a ligand in many, but not all, LFA-1-dependent adhesion reactions.
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TLDR
The results indicate that regulatory signals, which may function to modify homo- or heterotypic T cell adhesion as well as autocrine production of IL-2, can be transduced through CD43.
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